fluid and electrolyte balance in neurosurgery.pdf
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Presented by: Vikas Naik
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Introduction
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Introduction
Total body water 94% weight in early
gestation
Decreases to 78% at term
Reaches adult levels of 60% by 9 months
6/19/2009
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Objectives of IV Therapy
Maintain daily body fluid requirements
Restore previous body fluid losses
Replace present body fluid losses
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Average daily water balance of a
healthy adult (70 kg)
Intake outputBeverage 1200ml urine -1500ml
solid food 1000ml insens.loss- 900ml
Oxidation 300ml faces -100ml
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Fever Pyrexia increases insensible lossby about 20% for each C rise in bodytemperature
Ventilator
GI losses Equivalent volume of normalsaline added with potassium chloride use tocover the gastrointestinal fluid loss and fluidsequestrated in the bowel.
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Normal volume and composition of
body fluids
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Clinical parameters for evaluation of water balance
CVP
Pulse
Peripheral Veins
Weight Thirst
Intake and Output
Skin Edema
Lab Values
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Maintenance dose
For 24hrs
100ml/kg for 1-10kg
50ml/kg for 11-20
20ml/kg for 21-above
or 4ml/kg/hr for 1-10kg
2ml/kg/hr for 11-20
1ml/kg/hr for 21-above
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Pediatric neurosurgical patients over
24hrs
premature 90-100ml/kg
at term 80-90ml/kg
3m-1yr 70-80ml/kg>1yr 70ml/kg
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Effect on cerebral oedema formation
Effect on CPP Effect on glucose
Effect on electrolytes
6/19/2009
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IV fluids divided into crystalloid and colloid
depending on molecular weight of solutes
crystalloids 30,000mmol
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(5-964//+1,9:(5-964//+1,9:
!C8?86
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(+//+1,
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Plasma Derived Colloids
Plasma (FFP, cryoprecipitate)
- Coagulation problems only
Albumin
Plasma protein fraction/SHS
- Very expensive
- No proven benefit
- ? harmful
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ColloidsGELA
TINS
DEXTRA
NS
HES
Molecular
weight
28-35
kda
40-70
kda
70-450
kda
Advantages Improves
circulat
ion
Improvescirculatio
n
Improvescirculation,
endothelial
function
Anaphylaxsi
s
High small minimal
VOLUME
EFFECT
SHOR
T
MEDIUM LONGTER
M
COAGULA
TION
+/- ++ +
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Which Fluids ?
Depends on Nature of Loss!
Balanced approach for resuscitation:
2-3 crystalloid then colloid ? 0.9% saline or HS for head injuries
Ringers for other fluid resuscitation
Colloids included for major resuscitation Blood as needed for Hct = 30
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Crystalloid
Extracellar expander
Limited volume expansion
Maintain urine output Reduce plasma oncotic pressure
Variable electrolyte content
Cheap!
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Colloid
Advantages:
Intravascular expanders
Volume expansion
Rapid resuscitation
Maintain oncotic pressure
Less tissue oedema
Less pulmonary oedema
Disadvantages:
Coagulation problems
Variable electrolytecontent
Variable half-life
Adverse reactions
EXPENSIVE!
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#=7 !8;/078>7 +; (+//+1, ? (5-964//+1, +8 */++,#=7 !8;/078>7 +; (+//+1, ? (5-964//+1, +8 */++,@+/027:@+/027:
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1.Should not be used except fortreatment
of D. insipidus/ chronic SDH
2.Solution of 5% dextrose ishypoosmolar
3.RL is also slightly hypoosmolar,administration of >3 litres canreduce
plasma osmolality.!"#$"%&&$
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osmolality approximately that of plasma.
Eg: NS, Plasmalyte, and Normosol R. Hyperchloremic metabolic acidosis may
result with NS
!"#$"%&&$
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Usually Ringers lactate and/or Normal
Saline
- Avoid dextrose fluids
Infusion rate should be to replace urine
output and insensible losses ml. for ml.
Replace blood loss at 3:1 ratiocrystalloids or 1:1 of colloids downto
haematocrit of 25-30%!"#$"%&&$
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Permissible blood loss
EBV x (HIH
d) /H
I
EBV=weight x avg blood volume
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Increases plasma- cerebral parenchymaosmolality gradient
dose -0.5-2.0 gm/kg
large dose enhances cerebral bloodflow and free radicalscavenging
!"#$"%&&$
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Mechanism of action is similar to mannitol
Strengths of HS 3, 5 7.5%
Increases serum Na+ and hypokalemiacauses less diuresis
!"#$"%&&$
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Transfusion of blood in the form of packed cell ifHb< 8
Dilutional clinical coagulopathy when blood lossexceeds more than one blood volume
Fresh frozen plasma to be administered ifprothrombin time> 1.5 time normal
Dose of FFP: 10- 15 ml/ kg ( to obtain 30% ofplasma factor concentration)
Prophylactic administration contraindicated Platelet deficiency occurs if blood loss exceeds >
1.5 times EBV (14)
Transfusion indicated if counts less than 50,000/
cmm or if higher counts with bleeding!"#$"%&&$
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Dual set of problemsHypovolemia
Hyponatremia- CSW and SIADH
Avoid dehydration Cerebral vasospasm by
hypervolemia by CVP of 8- 10
hemodilution by PCV around 30-35
hypertension
Avoid dextrose containing solutions!"#$"%&&$
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Electrolytes
Normal values
Na+ - 130-149meq/l
K+ - 3.5-5meq/l
Cl- 95-110 meq/l
Ca- 8.1-10.4mg%
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Electrolyte Parenteral Equivalent
of RDA
Usual Intake
Sodium 12 meq/kg +
replacement,
but can be as
low as 540meq/d
Potassium 40100 meq/d
+ replacement
of unusual
lossesChloride As needed for acid-base
balance, but usually 2:1
to 1:1 with acetate
Acetate As needed for acid-base
balance
Calcium 10 meq 1020 meq/d
Factors controlling sodium Reabsorption
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Factors controlling sodium Reabsorption
in Perioperative Period
RAS:- Renin secretion
increases formation ofAngiotensin IIAldosterone Na reabsorption inDistal tubule
Sympathetic nervous system- IncreasedSympathetic activity increases sodium absorption inproximal tubule
ADH- it has little action on sodium excretion.,it
mostly maintains extracellular fluid volume
ANP- it is released from atrial cells & causesafferent arteriolar dilation & efferent arteriolar
constriction thus increasing GFR & natriuresis
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HYPONATREMIAHypovolumic Hypervolumic EuvolumicCCF
NEPHROTIC SYNDROME
RENAL FAILURE
CIRRHOSIS
Extra renal sodium loss
diarrhea
Vomiting
Blood loss
Excessive sweating
Renal sodium loss
CSWS
Diuretics
Osmotic diuresis
Adrenal insufficiency
ketonuria
SIADHCNS
SOL
Trauma
Hemorrhage
Stroke
Inflammatory
disordersdemyelination
DrugsCarbamazepine
Chlorpropramide
Phenothiazines
SRI
TCA
Pulmonaryconditions
Infections
ALI
Neoplasia
THIAZIDE DIURETICS
HYPOTHYROIDISMADRENAL
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Signs & Symptoms of HyponatremiaModerate-
lethargy
Nausea/vomiting
Irritability
HeadacheMuscle weakness/cramps
SevereDrowsiness
Depressed reflexesSeizures
Coma
Death
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Assesment of Pt with Hyponatremia
Clinical-
Skin turgor & mucous membranes
JVP
Orthostatic variation in pulse and B.P
daily wt.
Biochemical-
Serum Na+ & osmolarityUrine vol,S.G, Na+ & Osmolarity
BUN ,Cr,K+, Uric acid, Albumin,Cortisol
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HYPONATREMIA Contd
ECG features-
Mostly non specific
Appears when Na+< 115mmol/l
QRS widening,ST elevation,T inversion
Bradycardia, Ventricular ectopics also
possible
At values< 110mmol/l cardiac arrest mayoccur.
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Dose of Na+(meq)=wt(Kg)!(140-Na+)
!0.6
3%NS
Correction rate - 0.6-1mmol/l/hr tillNa=125meq/l
Half the deficit can be administered over 1st 8
hrs, rest over 1-3 days
Correct underlying disorder
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Hypertonic saline - symptomatic
Fluid restriction /Normal saline -
asymptomatic patients
Salt replacement
!"#$"%&&$
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Complication of Treatment
Pontine Myelinolysis - quadriparesis ,ataxia,abnormal extraocular movements. can occur with
rapid correction
Renal Failure, Peripheral edema, pulm
edema, heart failure
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SIADH
Diagnostic Criteria of SIADH:-!"##$%&!'( *+,$%%&-$. /001
Serum sodium serum osmolality
Normal thyroid, adrenal, renal function
Absence of peripheral edema ordehydration
Clinical features are same of hyponatremia
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Specific Treatment of SIADH
Fluid restriction- 1 l/day. (0.9% saline is usualchoice)
Furosemide
Lithium - blocks 3,5- AMP & inhibits action of ADHon renal tubule
Demeclocycline -900-1200 mg in divided doses,takes 3wks for maximal effect, Induces nephrogenicDI.
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Cerebral salt wasting
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Cerebral salt wasting
syndrome
Renal loss of sodium due to intracranialdisease, leading to hyponatremia &hypovolemia
Causes: Head injury
Brain tumor
Stroke Intracerebral hemorrhage
Tuberculous meningitis
Craniosynostosis repair
Cerebral salt wasting syndrome (
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Cerebral salt wasting syndrome (
CSWS )
Pathophysiology not fully understood-hypothesis
natriuretic response due to SNS overactivity
and DA release causes urinary sodium loss
release - brain natriuretic peptide, C-type
natriuretic peptide or an oubain like peptide,
by the injured brain
CSWS usually appears in the first week after
brain injury and spontaneously resolves in 2-
4 weeks
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Specific Treatment of CSWS
Fluid & Sodium Resuscitation -0.9%
saline used
acute symptomatic -hyponatremia 3%NS
Oral fludrocortisone - 0.1mg-0.4mg to
limit ve sodium balance in ptsrefractory to salt & fluid therapy
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Aneurysmal SAH
Abnormal sodium levels seen in acuteperiod(4-10days)
Incidence is 29%-43%2 3$+$#$'4 $5Neurolog res2000; 22:151-55, found
A.Com-51%-a/w hyponatremia
MCA-18% - a/w hyponatremia2 67%&.-$ et al -84% with hyponatremia had
symptomatic vasospasm2 ,$!$. '4 $5 8.. .'"%75 /009:;/?9didnt finddifference in mortality rates
Possible cause of hyponatremia is release of
BNP
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Transsphenoidal surgery for Pituitary Tumors
DI is Common CSW may commonly co-exist85*$.'!' '4 $5 @
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Surgery for Craniosynostosis
Frequently occurs, but usually
asymptomatic & transient
Etiology not conclusive
-could be SIADH a/w large fluid shifts
CSWS has also been reported byD$EE+
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>;A#$C&.$#)5&
Defined as serum Na >145mmol/l
Clinical variables:
1. Body weight
2. Peripheral oedema
3. CVP
4. Serum sodium/ Urine spot sodium
!"#$"%&&$
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Major causes of hypernatremia
CAUSES
Impaired Thirst
Solute (osmotic) diuresis
Excessive water loss Renal
Extrarenal
Combined disorders
MECHANISMS
Coma,
Essential Hypernatremia
Mannitol, DKA, Non ketotichyperosmolar coma
Pituitary DI,
Nephrogenic DI
Sweating
Coma + Hypertonic nasogastricfeeding
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>;A#$C&.$#)5&
Most s/s of hypernatrmia are
neurological
Altered mental status
Weakness
Neuromuscular irritability
Focal neurological deficit Occasional coma/seizures
Algorithim for assessment of Hypernatremia
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Algorithim for assessment of Hypernatremia
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Management of Hypernatremia
Goals Stop loss of water by T/t of cause
Correct water deficit
Water deficit can be calculated as
(S Na+-140/140)x TBW.
If serum glucose is elevated, then thecorrected formula is
S Na+=S Na++( S glu-90)/36As in hyponatremia, rapid correction ofhypernatremia is also dangerous
Management of Hypernatremia
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Management of Hypernatremia
Water deficit to be corrected over 48-72 hrs
No more than 0.5mmol/l/hr &12mmol/l/day
correction should be done
Safest method of correction is water by
mouth or NG tube.
If patient cannot take orally, 5% Dextrose canbe given intravenously
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!"#$"%&&$
DIABETUS INSIPIDUS
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Central DI
Nephrogenic DI
LC+5(#C+#*KML5CC#,$*-,$?5+&',C5.@&-%##C$#A*$.#(&-
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1/3rd in SAH and TBI1/6th in pituitary surgery and intracerebral
hemorrhage
CENTRAL DI:-It is a failure of release of ADH from
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It is a failure of release of ADH fromHypothalamo-pituitary axis
Characterised by inability to concentrateurine ,thus passage of large amount ofdilute urine
Rise in Plasma osmolality & progressive
dehydrationParticularly seen after pituitarysurgery,TBI, A Com Art aneurysmalSAH, & in brain death patients
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Etiology of Central DI
Acquired Head trauma
Post-pituitary surgery
Neoplasms Granulomas
Infections
Inflammations
Chemical toxins Tetrodoxins,Snake
venoms
Vascular
Idiopathic
Congenital Midline craniofacial
anomalies
Holoprosencephaly Ectopia of Pituitary
Genetic Autosomal dominant
Autosomal Recessive X-linked recessive
Deletionchromosome7q
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ETIOLOGY OF NEPHROGENIC DI
Vascular SCD
ATN
Granulomas
Neoplasm Infiltrations
Pregnancy
Idiopathic
GeneticX-linked recessive(ADH
receptorV2).
Autosomal Recessive(Aquaporin-2 gene)
Acquired
Drugs Lithium
Demeclocycline
Methoxyflurane Amphotericin B
Aminoglycoside
Cisplatin
Rifampicin
Foscarnet Metabolic
Hypercalcemia
Hypokalemia
Obstruction
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Rule out osmotic diuresis or fluid overload
Clinical signs and symptoms
Polyuria, abrupt high volumes (4 L/day18 L/day)
( within 2448 hours postoperatively)
Polydipsia, with craving for cold fluids
With/without hypovolemia
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ALGORITHM FOR DIAGNOSIS OF DI
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Treatment of postoperative
diabetes insipidusExpectant monitoring
I/O CHARTING
Urine osmolality or specific gravity every 4 to 6 hours,
Serum [Na+] every 4 to 6 hours
Antidiuretic hormone therapy
Desmopressin 1 mg to 2 mg iv/sc10mcg-20mcg nasal
Redose - urine output 200 mL to 250 mL/hr for 2 hours
with urine specific gravity < 1.005
urine osmolality < 200 mOsm/kg H2O
Maintenance
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drink according to thirst
Supplement hypotonic (D5W to D51/2NSS)
Monitor for resolution of transient DI or triphasic response
Positive daily fluid > 2 L suggests SIADH
Withhold -Antidiuretic hormone therapy
Manage anterior pituitary insufficiency
stress dose -hydrocortisone 100 mg TDS
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Chlorpropramide It acts by potentiating the action of AVP or activation
of V2 raceptors
Dose is 125-500mg OD
Onset slow, efficacy less,efficacy can be increasedby simultaneous use of Thizides.Hypoglycemia is asignificant side effect
Clofibrate & Carbamazepine is also helpful infew patients
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Nephrogenic DI:- T/t of cause & omitting the culprit drug
generally cures the disease
Thiazide Amiloride (esp in pts. On lithium)
Indomethacin
Low sodium diet
FLUID DEPRIVATION TEST
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FLUID DEPRIVATION TEST
Indication
Evaluation of Diabetes Insipidus
Precautions: Requires closemonitoring
Monitor urine output
Monitor vital signs
Monitor weight Do not allow weight loss to exceed
>3-5%
CONTD..
TechniqueFl id restrict patient
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Fluid restrict patient Mild polyuria (10 L/day) Start fluid restriction 2 hours before test
Follow Serum Osmolality to steady state
Serum Osmolality should approach 295 mOsmwater
Measure Serum Osmolality hourly until endpoint: Two values are within 30 mOsm of each other
Weight loss exceeds 3-5%
Administer endogenous ADH Vasopressin 5 units Sc
Intranasal DDAVP 10 ug
Measure Serum Osmolality 1 hour after ADH
administered
CONTD
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CONTD..
Interpretation Water deprivation effect on urine
concentrating ability
No response in Nephrogenic DI
No response in Central DI
Exogenous ADH effect on urineconcentrating ability
Corrects Central DI Does not correct Nephrogenic DI
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Hypokalemia
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Hypokalemia
Normal requirement 1meq/kg/day
Serum potassium < 3.5 mEq/ liter
Causes: intracellular shift
potassium depletion
6/19/2009
Hypokalemia
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Hypokalemia
Transcellular shift:beta agonists
diuretics
alkalosis
hypothermia
insulin !"#$%%&'()*+,*#&"-./*-$,,"%%*%.)&'/*%&%01$&,'/*
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Clinical features hypokalemia
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Clinical features hypokalemia
Muscle weakness and mental status
changes< 2.5 mEq/ liter ECG changes prominent U waves,
flattening and inversion of T waves,
prolonged QT interval Does not cause arrhythmias on its own
but definitely is proarrythmic
6/19/2009
Hypokalemia
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6/19/2009
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Management of hypokalemia
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Management of hypokalemia
Correct the primary causePotassium deficits in hypokalemia for 70
Kg malef4AEN S8?5CC
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Iv replacement
Potassium chloride- concentration varies from 1 and2 meq/ ml.
Extremely hyperosmololar and must be diluted
Infusion rate: add 20 meq to 100 ml isotonic saline
- rates of 20 mEq/ hour- can go as high as 40 mEq/ hour
- use central line with cardiac
monitoring
-If refractory check for magnesiumdeficiency as it promotes urinary lossesMild cases :Oral potassium chloride (1 TSF=20meq/l ),
2tsf TDS diluted in liquids
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Serum potassium > 5.5 mEq/ liter Most common cause is traumatic
hemolysis during venipuncture
20% blood sample incidence withelevated potassium
Source: transcellular shift ( urinary
K>30)
renal cause ( urinary K< 30)
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Slowing of electrical conduction of theheart
Usually starts when K level reaches 6.0
mEq/ L Tall tented T waves
Decrease in P wave amplitude
PR lengthening
QRS prolongation with eventual
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Management
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g
Guided by serum potassium and ECG
manifestation
1.Severe cases -Give 10 ml- 10% calciumgluconate over 5 minutes
Repeat second dose if necessary
No role for third doseAction lasts for 20 minutes
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2
. Insulin dextrose: 10 U regular insulin in500 ml 20% dextrose to infuse over 1 hour-decreases K by an average of 1 mEq/ L
3.Loop diuretics
4.Exchange resins
5.If refractory - hemodialysis
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Metabolic acidosis
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High Anion Gap
Renal failure
toxins
ketoacidosis
Normal anion gap (hyperchloremic)
Hyperkalemia
obstructive uropathy diarrhea
renal tubular acidosis
Some medications6/19/2009
Clinical features Headache
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Headache
Drowsiness Nausea/ vomiting/ diarrhea
Kussmauls respirations
Fruity-smelling breathe Hyperkalemia
Hypotension
Bradycardia GI distention
pH low (< 7.35)
HCO3 low (< 22)6/19/2009
Management:
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Management:
Fluid resuscitation Correct underlying disorder
Sodium bicarbonate only if pH< 7.20
Method: 0.5 x body weight x base deficit
correct half as slow infusion over few
minutes
other half to be repeated over 8 hours
repeat ABG values
stop when ph 7 206/19/2009
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Metabolic alkalosis
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Clinical features Shallow breathing
Nausea/vomiting/diarrhea
Confusion Numbness / tingling
Hypocalcemia
Hypokalemia
pH high (> 7.45)
HCO3 high (>26) cal features:6/19/2009
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Metabolic alkalosis
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Management: saline infusion (0.2*body
weight* chloride deficit)
In resistant cases give 0.1N HCl (0.5*
body weight* base excess)
Acetazolamide
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Respiratory acidosis and alkalosis
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Treatment of underlying cause
Correction of oxygenation
Sedation, reassurance and CO2
rebreathing for alkalosis
Ventilatory support and chest
physiotherapy
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